Chapter 3 Managing Pain With Therapeutic Modalities PDF

Chapter 3 Managing Pain With Therapeutic Modalities What is Pain? “An unpleasant sensory & emotional experience associated with actual or potential tissue damage, or described in terms of such damage” – The International Association for the Study of Pain Subjective sen...

Chapter 3 Managing Pain With Therapeutic Modalities What is Pain? “An unpleasant sensory & emotional experience associated with actual or potential tissue damage, or described in terms of such damage” – The International Association for the Study of Pain Subjective sensation Pain Perceptions – based on expectations, past experience, anxiety, suggestions Affective – one’s emotional factors that can affect pain experience Behavioral – how one expresses or controls pain Cognitive – one’s beliefs (attitudes) about pain Physiological response produced by activation of specific types of nerve fibers Experienced because of nociceptors being sensitive to extreme mechanical, thermal, & chemical energy. Composed of a variety of discomforts One of the body’s defense mechanism (warns the brain that tissues may be in jeopardy) Acute vs. Chronic – The total person must be considered. It may be worse at night when the person is alone. They are more aware of the pain because of no external diversions. Where Does Pain Come From? Cutaneous Pain – sharp, bright, burning; can have a fast or slow onset Deep Somatic Pain – stems from tendons, muscles, joints, periosteum, & b. vessels Visceral Pain – originates from internal organs; diffused @ 1st & later may be localized (i.e. appendicitis) Psychogenic Pain – individual feels pain but cause is emotional rather than physical Pain Sources Fast vs. Slow Pain – Fast – localized; carried through A-delta axons in skin Slow – aching, throbbing, burning; carried by C fibers Nociceptive neuron transmits pain info to spinal cord via unmyelinated C fibers & myelinated A-delta fibers. The smaller C fibers carry impulses @ rate of 0.5 to 2.0 m/sec. The larger A-delta fibers carry impulses @ rate of 5 to 30 m/sec. Acute vs. Chronic What is Referred Pain? Occurs away from pain site Example: Kerr’s sign Types of referred pain: Myofascial Pain – trigger points, small hyperirritable areas within a m. in which n. impulses bombard CNS & are expressed at referred pain Active – hyperirritable; causes obvious complaint Latent – dormant; produces no pain except loss of ROM Sclerotomic & Dermatomic Pain – deep pain; may originate from sclerotomic, myotomic, or dermatomic n. irritation/injury Sclerotome: area of bone/fascia that is supplied by a single n. root Myotome: m. supplied by a single n. root Dermatome: area of skin supplied by a single n. root Terminology Noxious – harmful, injurious Hyperesthesia – abnormal acuteness Noxious stimuli – stimuli that activate of sensitivity to touch, pain, or other nociceptors (pressure, cold/heat sensory stimuli extremes, chemicals) Paresthesia – abnormal sensation, Nociceptor – nerve receptors that such as burning, pricking, tingling transmits pain impulses Pain Threshold – level of noxious stimulus required to alert an individual Inhibition – depression or arrest of a of a potential threat to tissue function Pain Tolerance – amount of pain a Inhibitor – an agent that restrains/retards physiologic, chemical, or enzymatic action person is willing or able to tolerate Analgesic – a neurologic or pharmacologic state in which painful stimuli are no longer painful Accommodation phenomenon – adaptation by the sensory receptors to various stimuli over an extended period of time (e.g. superficial hot & cold agents). Less sensitive to stimuli. Questions to Ask about Pain Pattern: onset & duration Area: location Intensity: level Nature: description P-Q-R-S-T format Provocation – How the injury occurred & what activities   the pain Quality - characteristics of pain – Aching (impingement), Burning (n. irritation), Sharp (acute injury), Radiating within dermatome (pressure on n.)? Referral/Radiation – Referred – site distant to damaged tissue that does not follow the course of a peripheral n. Radiating – follows peripheral n.; diffuse Severity – How bad is it? Pain scale Timing – When does it occur? p.m., a.m., before, during, after activity, all the time Pain Assessment Scales Visual & Numeric Analog Scales None Severe 0 10 Locate area of pain on a pictures McGill pain questionnaire Evaluate sensory, evaluative, & affective components of pain 20 subcategories, 78 words McGill Pain Questionnaire 78 words that Completion may describe pain are take 20 minutes grouped into 20 sets and divided into 4 Administered categories every 2-4 weeks representing dimensions of the pain experience Goals In Managing Pain To control acute pain and protect patient from further injury while encouraging progressive exercise in a supervised environment. Reducing pain is an essential part of treatment Goals In Managing Pain Encourage body to heal through exercise designed to progressively increase functional capacity and to return the patient to work, recreational and other activities as swiftly and safely as possible Transmission of Pain Types of Nerves Neurotransmitters Types of Nerves Afferent (Ascending) – transmit impulses from the periphery to the brain First Order neuron Second Order neuron Third Order neuron Efferent (Descending) – transmit impulses from the brain to the periphery First Order Neurons Stimulated by sensory receptors End in the dorsal horn of the spinal cord Types A-alpha – non-pain impulses A-beta – non-pain impulses Large, myelinated Low threshold mechanoreceptor; respond to light touch & low- intensity mechanical info A-delta – pain impulses due to mechanical pressure Large diameter, thinly myelinated Short duration, sharp, fast, bright, localized sensation (prickling, stinging, burning) C – pain impulses due to chemicals or mechanical Small diameter, unmyelinated Delayed onset, diffuse nagging sensation (aching, throbbing) Neural Transmission (First Order Neurons) First order or primary afferents transmit impulses from the sensory receptor to the dorsal horn of the spinal cord Afferent First Order Neurons Second Order Neurons Receive impulses from the FON in the dorsal horn Lamina II, Substantia Gelatinosa (SG) - determines the input sent to T cells from peripheral nerve T Cells (transmission cells): transmission cell that connects sensory n. to CNS; neurons that organize stimulus input & transmit stimulus to the brain Travel along the spinothalmic tract Pass through Reticular Formation Types Wide range specific Receive impulses from A-beta, A-delta, & C Nociceptive specific Receive impulses from A-delta & C Ends in thalamus Neural Transmission (Second Order Neurons) Second order afferent fibers carry sensory messages from the dorsal horn to the brain Second order afferent fibers are categorized as wide dynamic range or nociceptive specific  Neural Transmission (Second Order Neurons) Wide dynamic range second order afferents receive input from A, A and C fibers. Second order afferents serve relatively large, overlapping receptor fields Nociceptive specific second order afferents respond exclusively to noxious stimulation Receive input only from A and C fibers Third Order Neurons Begins in thalamus Ends in specific brain centers (cerebral cortex) Perceive location, quality, intensity Allows to feel pain, integrate past experiences & emotions and determine reaction to stimulus Neural Transmission (Third Order Neurons) All of these neurons synapse with third order neurons which carry information to various brain centers where the input in integrated, interpreted and acted upon Descending Neurons Descending Pain Modulation (Descending Pain Control Mechanism) Transmit impulses from the brain (corticospinal tract in the cortex) to the spinal cord (lamina) Periaquaductal Gray Area (PGA) – release enkephalins Nucleus Raphe Magnus (NRM) – release serotonin The release of these neurotransmitters inhibit ascending neurons Stimulation of the PGA in the midbrain & NRM in the pons & medulla causes analgesia. Endogenous opioid peptides - endorphins & enkephalins Neurotransmitters Chemical substances that allow nerve impulses to move from one neuron to another Found in synapses Substance P - thought to be responsible for the transmission of pain- producing impulses Acetylcholine – responsible for transmitting motor nerve impulses Enkephalins – reduces pain perception by bonding to pain receptor sites Norepinephrine – causes vasoconstriction 2 types of chemical neurotransmitters that mediate pain Endorphins - morphine-like neurohormone; thought to  pain threshold by binding to receptor sites Serotonin - substance that causes local vasodilation &  permeability of capillaries Both are generated by noxious stimuli, which activate the inhibition of pain transmission Can be either excitatory or inhibitory Sensory Receptors Mechanoreceptors – touch, light or deep pressure Meissner’s corpuscles (light touch), Pacinian corpuscles (deep pressure), Merkel’s corpuscles (deep pressure) Thermoreceptors - heat, cold Krause’s end bulbs ( temp & touch), Ruffini corpuscles (in the skin) – touch, tension, heat; (in joint capsules & ligaments – change of position) Proprioceptors – change in length or tension Muscle Spindles, Golgi Tendon Organs Nociceptors – painful stimuli mechanosensitive chemosensitive Sensory Receptors Nerve Endings “A nerve ending is the termination of a nerve fiber in a peripheral structure.” (Prentice, p. 37) Nerve endings may be sensory (receptor) or motor (effector). Nerve endings may be: Respond to phasic activity - produce an impulse when the stimulus is  or , but not during sustained stimulus; adapt to a constant stimulus (Meissner’s corpuscles & Pacinian corpuscles) Respond to tonic receptors produce impulses as long as the stimulus is present. (muscle spindles, free n. endings, Krause’s end bulbs) Superficial – Merkel’s corpuscles/disks, Meissner’s corpuscles Deep – Pacinian corpuscles, Nerve Endings Merkel’s corpuscles/disks - Krause’s end bulbs – Sensitive to touch & vibration Thermoreceptor Slow adapting Ruffini corpuscles/endings Superficial location Thermoreceptor Most sensitive Sensitive to touch & tension Meissner’s corpuscles – Slow adapting Sensitive to light touch & Free nerve endings - vibrations Afferent Rapid adapting Detects pain, touch, temperature, Superficial location mechanical stimuli Pacinian corpuscles - Sensitive to deep pressure & vibrations Rapid adapting Deep subcutaneous tissue location Nociceptors Sensitive to repeated or prolonged stimulation Mechanosensitive – excited by stress & tissue damage Chemosensitive – excited by the release of chemical mediators Bradykinin, Histamine, Prostaglandins, Arachadonic Acid Primary Hyperalgesia – due to injury Secondary Hyperalgesia – due to spreading of chemical mediators Pain Control Theories Gate Control Theory Central Biasing Theory Endogenous Opiates Theory Gate Control Theory Melzack & Wall, 1965 Substantia Gelatinosa (SG) in dorsal horn of spinal cord acts as a ‘gate’ – only allows one type of impulses to connect with the SON Transmission Cell (T-cell) – distal end of the Second or neurons (SON) If A-beta neurons are stimulated – SG is activated which closes the gate to A-delta & C neurons If A-delta & C neurons are stimulated – SG is blocked which closes the gate to A-beta neurons Gate Control Theory Gate - located in the dorsal horn of the spinal cord Smaller, slower n. carry pain impulses Larger, faster n. fibers carry other sensations Impulses from faster fibers arriving @ gate 1st inhibit pain impulses (acupuncture/pressure, cold, heat, chem. skin irritation). Brain Pain Gate (T cells/ SG) Heat, Cold, Mechanical Gate Control Theory  Sensory information coming from A fibers is transmitted to higher centers in brain  “Pain message" carried along A & C fibers is not transmitted to second-order neurons and never reaches sensory centers Central Biasing Theory Descending neurons are activated by: stimulation of A-delta & C neurons, cognitive processes, anxiety, depression, previous experiences, expectations Cause release of enkephalins (PAG) and serotonin (NRM) Enkephalin interneuron in area of the SG blocks A-delta & C neurons Endogenous Opiates Theory Least understood of all the theories Stimulation of A-delta & C fibers causes release of B- endorphins from the PAG & NRM Or ACTH/B-lipotropin is released from the anterior pituitary in response to pain – broken down into B-endorphins and corticosteroids Mechanism of action – similar to enkephalins to block ascending nerve impulses Examples: TENS (low freq. & long pulse duration) Mechanisms of Pain Control The theories presented are only models Pain control is the result of overlapping mechanisms Useful in conceptualizing the perception of pain and pain relief  Pain Management Therapeutic modalities can be used to  Stimulate large-diameter afferent fibers( TENS, massage, analgesic balms)  Decrease pain fiber transmission velocity (cold, ultrasound)  Stimulate small-diameter afferent fibers and descending pain control mechanisms (accupressure, deep massage, TENS) Pain Management Therapeutic modalities can be used to  Stimulate release of endogenous opioids through prolonged small diameter fiber stimulation with TENS Goals in Managing Pain Reduce pain! Control acute pain! Protect the patient from further injury while encouraging progressive exercise Other ways to control pain Encourage central biasing – motivation, relaxation, positive thinking Minimize tissue damage Maintain communication w/ the athlete If possible, allow exercise Medications